Glycerolipids (triglyceride and phosphoglycerides) are essential for several liver functions including: The formation of very-low-density lipoproteins; proliferation, repair, and function of hepatocellular membranes, and the formation of biliary phospholipids. Therefore, identification of the factors which regulate hepatocellular glycerolipid metabolism and content (steady state relationship between degradation and formation) may be important in understanding the pathogenesis of liver disease and toxin-induced liver cell injury. Many toxin-related membrane injuries are caused by toxin metabolites. Microsomes are the major cellular site of toxin (CCl4, bromobenzene, etc.) metabolism and glycerolipid biosynthesis. Therefore, reactive toxin metabolites (generated by microsomes) may bind to microsomes (or other cellular membrane components) and initiate rapid alterations in membrane glycerolipid metabolism and content. Toxin-induced changes in hepatocellular glycerolipid content could disrupt membrane function and may represent an early event in toxin-dependent cell injury. Hence, these studies are designed to correlate toxin-related changes in hepatocellular glycerolipid metabolism with toxin-dependent alterations in membrane structure and function in whole animals, isolated hepatocytes, hepatocyte monolayers, and subcellular fractions.